HPA3和传统危险因素在急性心肌梗死的交互作用

Interaction between Human Platelet Alloantigens3 and Traditional Risk Factors in Acute Myocardial Infarction

【目的】探讨人类血小板抗原(HPA3)基因多态性与传统危险因素在急性心肌梗死(AMI)的交互作用。【方法】选择215例AMI患者和210例健康体检者作为研究对象,采用序列特异性引物-多聚酶链反应(SSP-PCR)技术扩增目的基因,进行HPA基因分型,分析其在AMI中的危险因素,使用叉生分析法分析HPA3基因与传统危险因素在AMI中的交互作用。【结果】①HPA3基因多态性在AMI组和对照组的分布差异无统计学意义(P>0.05);②HPA3b等位基因与年龄≤60岁对AMI发病不存在交互作用(OR=1.361,95%CI=0.824-2.250);HPA3b等位基因与有吸烟史、伴高血压、糖尿病或血脂异常病史对AMI发病存在拮抗作用(OR=0.238,95%CI 0.130～0.436;OR=0.415,95%CI 0.248～0.695;OR=0.279,95%CI0.122～0.640;OR=0.372,95%CI 0.212～0.654)。【结论】HPA3b等位基因在AMI发病中的作用可能与有吸烟史、伴高血压、糖尿病或血脂异常病史相互抵消。

[ Objective ] To analyze the interaction between human platelet alloantigens3 （HPA3） and traditional risk factors in acute myocardial infarction （AMI）. [ Methods ] The study consisted of 215 AMI patients, the controls were selected form healthy people. Total genomic DNA was isolated by the phenol-chloroform method, and HPA genotyping was done by the polymerase chain reaction method using sequence-specific primers. Meanwhile, regression analysis was applied in assessing the genetic risk factors to AMI. The method of crossover analysis was used to study the interaction between human platelet aUoantigens3 and traditional risk factors in AMI. [Results] （1） Compared with the control group, the difference of HPA3 gene polymorphism were not statistically significant （P 〉 0.05）. （2） Compared with control group, there were no interaction in HPA3b allele with age （≤60） （OR = 1.361, 95%CI = 0.824-2.250）, and interaction analysis confirmed the abated negative association of HPA3b allele with smoking （OR= 0.238, 95%CI 0.130-0.436）, hypertension （0R=0.415, 95%CI 0.248- 0.695）, diabetes （0R=0.279, 95%CI 0.122-0.640） or dyslipidemia （0R=0.372, 95%CI 0.212-0.654）. [Conclusion]There may show abated negative association of the HPA3b allele with smoking, hypertension, diabetes, or dyslipidemia in AMI.